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Proc Natl Acad Sci U S A. 2013 Apr 16;110(16):6459-64. doi: 10.1073/pnas.1304432110. Epub 2013 Apr 3.

Rig-I regulates NF-κB activity through binding to Nf-κb1 3'-UTR mRNA.

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State Key Laboratory of Medical Genomics, Research Center for Experimental Medicine, Shanghai Institute of Hematology, Rui-Jin Hospital- Shanghai Jiao Tong University School of Medicine, SJTUSM, Shanghai 200025, China.


Retinoic acid inducible gene I (RIG-I) senses viral RNAs and triggers innate antiviral responses through induction of type I IFNs and inflammatory cytokines. However, whether RIG-I interacts with host cellular RNA remains undetermined. Here we report that Rig-I interacts with multiple cellular mRNAs, especially Nf-κb1. Rig-I is required for NF-κB activity via regulating Nf-κb1 expression at posttranscriptional levels. It interacts with the multiple binding sites within 3'-UTR of Nf-κb1 mRNA. Further analyses reveal that three distinct tandem motifs enriched in the 3'-UTR fragments can be recognized by Rig-I. The 3'-UTR binding with Rig-I plays a critical role in normal translation of Nf-κb1 by recruiting the ribosomal proteins [ribosomal protein L13 (Rpl13) and Rpl8] and rRNAs (18S and 28S). Down-regulation of Rig-I or Rpl13 significantly reduces Nf-κb1 and 3'-UTR-mediated luciferase expression levels. These findings indicate that Rig-I functions as a positive regulator for NF-κB signaling and is involved in multiple biological processes in addition to host antivirus immunity.

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